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Invivo, oral gavage with the synthetic, specific FFAR4 agonist CpdB decreased the level of circulating NEFAs in fasting lean mice to a similar degree as nicotinic acid. In agreement with the identified anti-lipolytic effect of FFAR4, plasma NEFAs and glycerol were increased in FFAR4-deficient mice as compared to littermate controls despite having elevated insulin levels, and cAMP accumulation in primary adipocyte cultures was augmented by treatment with the FFAR4 antagonist conceivably by blocking the stimulatory tone of endogenous NEFAs on FFAR4.<br />In white adipocytes, FFAR4 functions as an NEFA-activated, autocrine, negative feedback regulator of lipolysis by decreasing cAMP though Gi-mediated signaling.<br />In white adipocytes, FFAR4 functions as an NEFA-activated, autocrine, negative feedback regulator of lipolysis by decreasing cAMP though Gi-mediated signaling.CD44 and the receptor for hyaluronic acid-mediated motility (RHAMM) are the main hyaluronan (HA) receptors. They are commonly overexpressed in different cancers activating signaling pathways related to tumor progression, metastasis and chemoresistance. Besides their involvement in signal transduction via interaction with HA, currently, there is a little information about the possible crosstalk between CD44 and RHAMM and the role of HA in this process. In the present work, we used immunocytochemistry combined with Förster resonance energy transfer (FRET) microscopy and co-immunoprecipitation to elucidate the involvement of HA in CD44 and RHAMM expression, co-localization and crosstalk. We studied breast cancer cells lines with different degrees of invasiveness and expression of these receptors in the absence of exogenous HA and compared the data with the results obtained for cultures supplemented with either soluble HA or seeded on substrates with end-on immobilized HA. Our results demonstrated that cells response depends on the HA presentation CD44/RHAMM complexation was upregulated in all cell lines upon interaction with immobilized HA, but not with its soluble form. Moreover, the results showed that the expression of both CD44 and RHAMM is regulated via interactions with HA indicating cell-specific feedback loop(s) in the signaling cascade.Proper microstructural and transport properties are fundamental requirements for a suitable scaffold design and realization in tissue engineering applications. Scaffold microstructure (i.e. pore size, shape and distribution) and transport properties (i.e. intrinsic permeability), are commonly recognized as the key parameters related to the biological performance, such as cell attachment, penetration depth and tissue vascularization. [https://www.selleckchem.com/products/ginsenoside-rg1.html Ginsenoside Rg1] While pore characteristics are relatively easy to asses, accurate and reliable evaluation of permeability still remains a challenge. In the present study, the microstructural properties of foam-replicated bioactive glass-derived scaffolds (basic composition 47.5SiO2-2.5P2O5-20CaO-10MgO-10Na2O-10K2O mol.%) were determined as function of the sintering temperature within the range 600-850°C, identified on the basis of thermal analyses that were previously performed on the material. Scaffolds with total porosity between 55 and 84 vol.% and trabecular-like architecture were obtained, with pore morphological features varying according to the sintering temperature. Mathematical modelling, supported by micro-computed tomography (μ-CT) imaging, was implemented to selectively investigate the effect of different pore features on intrinsic permeability, which was determined by laminar airflow alternating pressure wave drop measurements and found to be within 0.051-2.811·10-10 m2. The calculated effective porosity of the scaffolds was in the range of 46 to 66 vol.%, while the average pore diameter assessed by μ-CT varied between 220 and 780 μm, where the values in the lower range were observed for higher sintering temperatures (750-850°C). Experimental results were critically discussed by means of a robust statistical analysis. Finally, the complete microstructural characterization of the scaffolds was achieved by applying the general constitutive equation based on Forchheimer's theory.Implant-associated infection (IAI) induced by methicillin-resistant Staphylococcus aureus (MRSA) is a devastating complication in the orthopedic clinic. Traditional implant materials, such as Ti6Al4V, are vulnerable to microbial infection. In this study, we fabricated a copper (Cu)-containing titanium alloy (Ti6Al4V-Cu) for the prevention and treatment of MRSA-induced IAI. The material characteristics, antibacterial activity, and biocompatibility of Ti6Al4V-Cu were systematically investigated and compared with those of Ti6Al4V. Ti6Al4V-Cu provided stable and continuous Cu2+ release, at a rate of 0.106 mg/cm2/d. Its antibacterial performance against MRSA in vitro was confirmed by plate counting analysis, crystal violet staining, and scanning electron microscopic observations. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis demonstrated that Ti6Al4V-Cu suppressed biofilm formation, virulence, and antibiotic-resistance of MRSA. The in vivo anti-MRSA effect was investigated in a rat IAI model. Implants were contaminated with MRSA solution, implanted into the femur, and left for 6 weeks. Severe IAI developed in the Ti6Al4V group, with increased radiological score (9.6 ± 1.3) and high histological score (10.1 ± 1.9). However, no sign of infection was found in the Ti6Al4V-Cu group, as indicated by decreased radiological score (1.3 ± 0.4) and low histological score (2.3 ± 0.5). In addition, Ti6Al4V-Cu had favorable biocompatibility both in vitro and in vivo. In summary, Ti6Al4V-Cu is a promising implant material to protect against MRSA-induced IAI.<br />The fragile X mental retardation protein (FMRP) affects multiple steps of the mRNA metabolism during brain development and in different neoplastic processes. However, the contribution of FMRP in colon carcinogenesis has not been investigated.<br />FMR1 mRNA transcript and FMRP protein expression were analyzed in human colon samples derived from patients with sporadic colorectal cancer (CRC) and healthy subjects. We used a well-established mouse model of sporadic CRC induced by azoxymethane to determine the possible role of FMRP in CRC. To address whether FMRP controls cancer cell survival, we analyzed cell death pathway in CRC human epithelial cell lines and in patient-derived colon cancer organoids in presence or absence of a specific FMR1 antisense oligonucleotide or siRNA.<br />We document a significant increase of FMRP in human CRC relative to non-tumor tissues. Next, using an inducible mouse model of CRC, we observed a reduction of colonic tumor incidence and size in the Fmr1 knockout mice. The abrogation of FMRP induced spontaneous cell death in human CRC cell lines activating the necroptotic pathway.